Metabolic regulation of calcium in blood is absolutely essential for survival, and the concentration is maintained constant quite strictly. When the blood calcium concentration is increased by some reason, it causes various diseases such as hypertension, arteriosclerosis, diabetes, myocardial infarction, and hypercalcemia. On the other hand, decrease in blood calcium concentration also results in diseases such as hypocalcemia. In addition, substantial decrease in blood calcium concentration due to, for example, massive hemorrhage or radiation exposure may sometimes lead to death.
As cells responsible for quite important regulation of blood calcium concentration, which is quite important in vivo, osteoclast is presently known. Osteoclast is considered to directly regulate the calcium concentration in blood by resorbing bone (bone matrix) and releasing calcium into blood. In mammals, however, there are only about 50,000 osteoclasts in vivo. On the contrary, there are about 25,000 osteocytes, even in 1 mm.sup.3 of bone, embedded in calcified hard tissues reserving calcium. Population of osteoclasts is therefore considered too small to regulate the calcium concentration in blood (Kumegawa et al., Molecular Medicine, 30, p.1254 (1993) and Ozawa et al., Nihon-Rinsho, vol. 52, No. 9, p. 2246 (1994)).
Furthermore, because there are no osteoclasts in op/op mouse which is a model animal for osteopetrosis, the primary function of osteoclast, bone remodeling, scarcely occurs in this animal. Despite the absence of osteoclast, however, the blood calcium concentration is maintained normally in this animal (Molecular Medicine, Vol. 30, No. 10, p. 1240 (1993)).
This fact suggests that the regulation of the blood calcium concentration by osteoclast is just supplemental and there may exist some other cells which dominantly regulate the calcium concentration in blood. Although such cells have not yet been identified, if any factors which grow such cells or which induce cells to produce such cells are found, the factors themselves or inhibitors thereof are expected to be useful as therapeutic agents for various diseases caused by abnormality in blood calcium concentration as described above. Although identification of such factor has been desired, its successful cloning has not yet been reported.